lipoproteinmetabolism

Lipoprotein metabolism refers to the processes by which lipids are transported through the circulation within lipoprotein particles, remodeled, and ultimately delivered to or removed by tissues. This system coordinates the production, maturation, lipolysis, and clearance of lipoproteins that carry triglycerides and cholesterol. Key players include chylomicrons, very-low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL), each defined by specific apolipoproteins and lipid compositions.

Chylomicrons are formed in enterocytes after dietary fat intake, containing ApoB-48, ApoC-II, and ApoE. They deliver triglycerides to peripheral tissues via lipoprotein lipase (LPL), releasing fatty acids and generating chylomicron remnants, which are cleared by the liver after ApoE-mediated receptor uptake. The liver also produces VLDL, rich in triglycerides and containing ApoB-100; VLDL is remodeled by LPL to form IDL and then LDL. LDL, enriched in cholesterol esters, is taken up primarily by hepatic and peripheral LDL receptors, delivering cholesterol to cells. HDL participates in reverse cholesterol transport, accepting cholesterol from tissues (often aided by ApoA-I and ABCA1) and delivering it to the liver, aided by LCAT and selective uptake via SR-BI.

Remodeling enzymes such as cholesteryl ester transfer protein (CETP) exchange triglycerides and cholesteryl esters among lipoproteins, influencing particle composition and clearance. Apolipoproteins regulate interactions with receptors: ApoB-48 on chylomicrons, ApoB-100 on VLDL/LDL, ApoE for remnant uptake, and ApoC-II as a cofactor for LPL.

Dysregulation of lipoprotein metabolism contributes to hyperlipidemias and atherosclerosis. Measurement of lipoprotein subclasses and apolipoproteins aids diagnosis and risk assessment.